FDA approved psoriasis drug could prevent Type 1 diabetes, study finds

In type 1 diabetes, the body’s own immune system turns against the pancreas. Cells meant to protect you start destroying insulin-producing beta cells. This damage leads to a lifelong need for insulin therapy and strict monitoring of blood sugar levels to avoid serious health problems. A recent breakthrough may change that outlook.

Researchers have uncovered a new way to slow or even prevent the destruction of these vital cells. It involves a protein called tyrosine kinase 2, or TYK2, that helps drive the inflammation behind the disease. When TYK2 activity is blocked, inflammation decreases and beta cells survive longer. That could make a major difference for people at risk or recently diagnosed with the disease.

When type 1 diabetes develops, immune cells invade the pancreas and create a cycle of inflammation and destruction. These cells release signals known as cytokines, which stir up more immune activity and lead to the death of insulin-producing beta cells. One protein, TYK2, plays a key role in relaying these signals. It activates STAT1 and STAT2, which are transcription factors that tell cells how to respond.

Scientists have found that certain changes, or mutations, in the TYK2 gene can lower the risk of autoimmune diseases like type 1 diabetes, rheumatoid arthritis, and ulcerative colitis. These genetic changes reduce TYK2’s activity, slowing the harmful signals and easing immune attacks.

TYK2 helps transmit signals from three major cytokines: interferon-alpha (IFNα), interleukin-12, and interleukin-23. Each of these has been linked to autoimmune conditions, but IFNα plays the biggest role in type 1 diabetes. This signal shows up early, even before symptoms appear, in kids who are genetically at risk. It also appears in the blood and pancreas of people just diagnosed with the disease.

IFNα activates immune cells that live in the pancreas, such as macrophages and T cells. It also stresses the beta cells, pushing them toward death. Studies have shown that when human beta cells are exposed to IFNα, they start showing signs of stress and inflammation. Their gene activity changes, their protective outer layers become overactive, and their internal processes start to break down.

There have even been cases where people developed type 1 diabetes after being treated with IFNα for hepatitis C or leukemia. On the other hand, blocking IFNα or its main receptor has prevented diabetes in lab animals. These findings point to TYK2—and its role in IFNα signaling—as a prime target for new therapies.

Medications that block TYK2 may offer a safer way to reduce immune attacks without the risks tied to other drugs. Traditional JAK inhibitors, which also block similar inflammation pathways, have been linked to blood clots, heart problems, and cancer, especially in older adults. TYK2 inhibitors work more selectively and seem to avoid these side effects.

In 2022, a drug called deucravacitinib was approved by the U.S. Food and Drug Administration to treat psoriasis. This medication targets TYK2 in a way that stops its ability to relay harmful cytokine signals. That same mechanism could help protect beta cells in people with type 1 diabetes.

Early lab tests using human cells and mouse models showed that TYK2 inhibitors, such as BMS-986165 and BMS-986202, could block the effects of IFNα. These drugs reduced immune cell activity, lowered stress in beta cells, and even delayed the start of diabetes in animals. They also cut down on the damaging interactions between T cells and beta cells.

To explore this further, researchers used in situ spatial transcriptomics—a tool that shows which genes are active in specific locations inside tissues. The results confirmed that TYK2 inhibitors calm both the innate and adaptive branches of the immune system. They also directly protect the insulin-producing cells that type 1 diabetes targets.

The research was led by a team from Indiana University School of Medicine and was published in eBioMedicine. It was co-led by Dr. Carmella Evans-Molina, director of the Indiana Diabetes Research Center, and Dr. Farooq Syed, now at the City of Hope in California. They believe the treatment could offer a powerful new tool.

“Our study showed that targeting TYK2 could be a powerful way to protect insulin-producing beta cells while calming inflammation in the immune system at the same time,” said Dr. Evans-Molina. “This finding is exciting because there is already a drug on the market that does this for psoriasis, which could help us move more quickly toward testing it for Type 1 diabetes.”

Dr. Syed added, “Our preclinical models suggest that the treatment might work in people as well. The next step is to initiate translational studies to evaluate the impact of TYK2 inhibition alone or in combination with other already approved drugs in individuals at risk or with recent onset Type 1 diabetes.”

This research was supported by a large international team. Members came from the Université Libre de Bruxelles, the Indiana Biosciences Research Institute, Leiden University Medical Center, the University of Pisa, and Purdue University. Each group contributed data and expertise to build a strong case for future human trials.

Among the study’s authors were Chih-Chun Lee, Jyoti Rana, Preethi Krishnan, Staci Weaver, and others from Indiana University. International contributors included Olivia Ballew, Alexandra Coomans de Brachène, Sofia Thomaidou, Lorella Marselli, and Jing Liu.

Their goal is to move these findings into clinical settings, where they can be tested safely in people with early-stage type 1 diabetes or those at high risk. Because the drug is already FDA-approved for psoriasis, researchers may be able to launch human trials faster than usual.

The science behind TYK2 inhibition offers a rare mix of promise and practicality. By targeting a pathway that’s central to the immune system’s attack on beta cells, this approach could delay or prevent the onset of type 1 diabetes. And because the drug already exists, the path to human testing may be shorter than for many new treatments.

If successful, TYK2 blockers could change how doctors approach type 1 diabetes. Instead of only managing blood sugar, they might be able to preserve the cells that produce insulin in the first place. That would represent a huge shift—one rooted in years of careful research, global collaboration, and a new understanding of the immune system’s inner workings.

Note: The article above provided above by The Brighter Side of News.

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